ORIGINAL ARTICLE
Vimentin 3 expression in odontogenic keratocysts – a molecular and immunohistochemical study
1
Department of Oral Pathology, Faculty of Dentistry, Gazi University, Ankara, Turkey
2
Institute of General Pathology and Pathological Anatomy, Faculty of Medicine, University Hospital Cologne,
Cologne, Germany
3
Clinic and Polyclinic for Urology, Faculty of Medicine, University Hospital Cologne, Cologne, Germany
Submission date: 2025-10-27
Final revision date: 2025-11-19
Acceptance date: 2025-12-02
Publication date: 2026-02-04
Corresponding author
Sibel Elif Gültekin
Prof. Dr. Sibel Elif Gültekin Department of Oral Pathology Faculty of Dentistry Gazi University Ankara, Turkey
Prof. Dr. Sibel Elif Gültekin Department of Oral Pathology Faculty of Dentistry Gazi University Ankara, Turkey
Pol J Pathol 2025;76(4):284-291
KEYWORDS
TOPICS
ABSTRACT
Odontogenic keratocysts (OKC) are locally aggressive jaw lesions characterized by a high recurrence rate. Vimentin 3 (VIM3), a truncated splice variant of full-length vimentin (VIMFL), has recently emerged as a potential biomarker in odontogenic tumors.
However, its role in OKC and association with recurrence remain unexplored. Formalin-fixed paraffin-embedded samples from OKC (n = 25) and dentigerous cysts (DC) (n = 25) were analyzed. Immunohistochemical staining for VIM3, VIMFL, p53, and Ki-67 was performed. In parallel, reverse transcription-quantitative polymerase chain reaction was used to assess mRNA expression levels of VIM3, VIMFL, and p53.
While VIM3 expression did not significantly differ between OKC and DC, recurrent OKC exhibited significantly higher VIM3 labeling indices compared to non-recurrent cases (p = 0.040).
This study demonstrates, for the first time, the expression of VIM3 in OKC. Although the findings are promising, further research with larger cohorts and functional validation is required to clarify the mechanistic role of VIM3 in odontogenic cyst biology.
However, its role in OKC and association with recurrence remain unexplored. Formalin-fixed paraffin-embedded samples from OKC (n = 25) and dentigerous cysts (DC) (n = 25) were analyzed. Immunohistochemical staining for VIM3, VIMFL, p53, and Ki-67 was performed. In parallel, reverse transcription-quantitative polymerase chain reaction was used to assess mRNA expression levels of VIM3, VIMFL, and p53.
While VIM3 expression did not significantly differ between OKC and DC, recurrent OKC exhibited significantly higher VIM3 labeling indices compared to non-recurrent cases (p = 0.040).
This study demonstrates, for the first time, the expression of VIM3 in OKC. Although the findings are promising, further research with larger cohorts and functional validation is required to clarify the mechanistic role of VIM3 in odontogenic cyst biology.
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| eISSN: | 2084-9869 |
| ISSN: | 1233-9687 |
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